DNMT3A
DNA methyltransferase 3 alpha
Gene summary
A protein-coding gene on chromosome 2 (epigenetic regulation). CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. Studies in mice have demonstrated that DNA methylation is required for mammalian development.
Source: NCBI Gene, accessed 2026-10-07.
Protein reference (UniProt)
- Protein
DNA (cytosine-5)-methyltransferase 3A
- Function
Required for genome-wide de novo methylation and is essential for the establishment of DNA methylation patterns during development. DNA methylation is coordinated with methylation of histones. It modifies DNA in a non-processive manner and also methylates non-CpG sites. May preferentially methylate DNA linker between 2 nucleosomal cores and is inhibited by histone H1 (By similarity). Plays a role in paternal and maternal imprinting (By similarity). Required for methylation of most imprinted loci in germ cells (By similarity). Acts as a transcriptional corepressor for ZBTB18 (By similarity). Recruited to trimethylated 'Lys-36' of histone H3 (H3K36me3) sites (By similarity). Can actively repress transcription through the recruitment of HDAC activity (By similarity). Also has weak auto-methylation activity on Cys-710 in absence of DNA (By similarity).
- Subcellular location
Nucleus; Chromosome; Cytoplasm.
- Tissue specificity
Highly expressed in fetal tissues, skeletal muscle, heart, peripheral blood mononuclear cells, kidney, and at lower levels in placenta, brain, liver, colon, spleen, small intestine and lung.
- Associated conditions
Tatton-Brown-Rahman syndrome (TBRS); Leukemia, acute myelogenous (AML); Heyn-Sproul-Jackson syndrome (HESJAS).
Source: UniProtKB/Swiss-Prot Q9Y6K1, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.
Why its pathway is in the library
Epigenetic persistence is the leading hypothesis for why post-drug syndromes endure after the drug is gone; chromatin regulators are therefore priority candidates in any persistence mechanism.
Written for the whole epigenetic regulation family, not for DNMT3A specifically.
Mentioned in 1 corpus record
- Conference abstract
Epigenetic Modulation of ESR1 and DNMT3A Following Finasteride Exposure: Implications for Female Reproductive Function
Churchill Jonadab Ihentuge · Physiology (Physiology Summit meeting abstract)
Conference abstract reporting epigenetic modulation of ESR1 (estrogen receptor alpha) and DNMT3A (DNA methyltransferase 3A — part of the epigenetic machinery itself) following finasteride exposure, framed around female reproductive function. Finasteride…
DNMT3AESR1EPI-0102026PFSEpigenetics supplement · Oct 2026
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